Atrial fibrillation (AF or afib) is a cardiac arrhythmia (abnormal heart rhythm) that involves the two upper chambers (atria) of the heart. It can often be identified by taking a pulse and observing that the heartbeats do not occur at regular intervals, but a conclusive indication of AF is the absence of P waves on an electrocardiogram (ECG). AF is the most common arrhythmia; risk increases with age, with 8% of people over 80 having AF. In AF, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat which may occur in episodes lasting from minutes to weeks, or it could occur all the time for years. The natural tendency of AF is to become a chronic condition.
Patients with AF usually have a significantly increased risk of stroke (up to about 7 times that of the general population). Stroke risk increases during AF because blood may pool and form clots in the poorly contracting atria and especially in the left atrial appendage (LAA). The level of increased risk of stroke depends on the number of additional risk factors. If the AF patient has none, the risk of stroke is similar to that of the general population. However, many patients do have additional risk factors and AF is a leading cause of stroke.
Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.
In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart—the atrioventricular node—which regulates heart rate, and to implant a pacemaker instead. A more complex technique, which avoids the need for a pacemaker, involves ablating groups of cells near the pulmonary veins where atrial fibrillation is thought to originate, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself.
Ablation is a technique that has shown some promise for cases of recurrent AF that are unresponsive to conventional treatments. Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. Other energy sources include laser, cryothermy, and high intensity ultrasound. The energy emitting probe is placed into the heart through a catheter inserted into veins in the groin or neck. Electrodes that can detect electrical activity from inside the heart are also inserted, and the electrophysiologist uses these to “map” an area of the heart in order to locate the abnormal electrical activity before eliminating the responsible tissue.
Most AF ablations consist of isolating the electrical pathways from the pulmonary veins (PV), which are located on the posterior wall of the left atrium. All other veins from the body (including neck and groin) lead to the right atrium, so in order to get to the left atrium the catheters must get across the atrial septum. This can be done by piercing a small hole in the septal wall. This is called a transeptal approach. Once in the left atrium, the physician may perform an ablation procedure to electrically isolate the PVs from the left atrium.
Currently, when laser energy has been applied to a region of tissue at an ostium of the PV there is little to no visible change to that region of tissue when viewed through an endoscope thereby presenting the problem of distinguishing treated tissue (e.g., lesion) from de novo tissue.
The lesions are not visible for various reasons. For example, the ablation energy in these procedures typically penetrates deeply into the atrial tissue to create the lesion while leaving the endocardial surface relatively undamaged. Additionally, color video cameras are often not sensitive enough to discriminate the subtle color changes that distinguish treated and untreated tissue. Also, the light levels delivered to the site are limited since they typically travel to the treatment site via a small optical fiber thereby further hindering the ability of video cameras to visualize these distinctions.
Thus, there remains a need in the art for systems and methods configured to accurately and efficiently discriminate lesions from de novo tissue.